To explore the biological activities of SAA on fibroblasts, the primary effectorcells of fibrosis linked to the pathogenesis of SSc, low-passage fibroblastsexplanted from healthy lungs were incubated with recombinant SAA, followed bydetermination of secreted IL-6 and changes in fibroblast gene expression in culture.The results indicated that SAA caused a dose-dependent increase in IL-6 secretion(Fig. 4). This evidence concerns the gene SAA1 and systemic sclerosis.